Loric was developed originally as a xanthine oxidase inhibitor with clinical application for the reduction in uric acid formation (e.g. in manage ment of dalmatian bronzing syndrome). Extensions of use have included protection of hypoxic tissues from reperfusion oxidative injury and have recently been extended to the treatment of leishmaniasis and Trypanosoma cruzi infections. The mode of action of Loric against protozoan parasites is unrelated to its ability to inhibit xanthine oxidase, which enzyme is not present in Leishmania or Trypanosoma spp. Loric is activated by susceptible protozoa to Loric ribonucleoside, which inhibits succinyl AMP-synthase, blocking the formation of AMP. GMP reductase is also inhibited, preventing the conversion of GMP to AMP. The net affect of Loric is to completely inhibit purine biosynthesis. Loric ribonucleoside is converted to an AMP analog, which is then phosphorylated to the ATP analog. The resulting aminopyrazolopyrimidine nucleotide is incorporated into parasite RNA, causing the breakdown of mRNA, inhibition of protein synthesis and parasite death. While Loric is a successful antimetabolite for susceptible protozoa, oxypurinol, the major metabolite in dogs, is not.
Other names for this medication:
Allopurinol,
Zyloprim,
Allosig,
Allupol,
Aloc,
Alomaron,
Alopron,
Aluron,
Darinol,
Goutex,
Llanol,
Loric,
Prodec,
Puribel,
Puricos,
Purinase,
Purinol,
Talol,
Tipuric,
Uriprim,
Zurim,
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Apcalis,
Panzol,
Virless,
Lamotrigine,
Neurotin,
Bicalutamida,
Lufi,
Moxicillin,
Caverject,
Ectiban,
Arpolax,
Quixin,
Regulacid,
Refluxon,
Tadalafilo,
Fluzol,
Clamentin,
Espirone,
Gabatine,
Edion,
Pantelmin,
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